P. Herpin et al., EFFECT OF THYROID STATUS IN THE PERINATAL-PERIOD ON OXIDATIVE CAPACITIES AND MITOCHONDRIAL RESPIRATION IN PORCINE LIVER AND SKELETAL-MUSCLE, Reproduction, fertility and development, 8(1), 1996, pp. 147-155
Regulatory thermogenesis is reduced in newborn piglets which have been
made hypothyroid during late gestation by giving the sow a high gluco
sinolate rapeseed diet (test animals). Thereafter, the progressive inc
rease in thermogenic capacity parallels the development of a marked po
stnatal hyperthyroid state. To explain these effects of thyroid hormon
es at the tissue and mitochondrial levels, we have examined both liver
and skeletal muscle to determine possible underlying changes in (i) t
issue oxidative capacities (cytochrome oxidase (GO) activity), between
80 d of gestation and 48 h after birth, and (ii) mitochondrial conten
t and respiratory capacities at 24 h of life. In control piglets, CO a
ctivity increased sharply during late gestation and the first 2 d of l
ife in liver and rhomboideus (RH) muscle (P < 0.01), whereas only a pr
enatal increase was observed in longissimus dorsi (LD) muscle. Test fe
tuses were hypothyroid and had lower CO activities than controls durin
g late gestation in RH muscle (P < 0.06, at 110 d of gestation; P < 0.
08, at birth) and in liver (P < 0.001, at birth). The postnatal increa
se in CO activity in RH muscle and liver was higher (P < 0.05) in test
than in control piglets, and as a result the difference between the 2
groups was not significant by 24-48 h of life. There was no effect of
treatment on LD muscle. At 24 h, hyperthyroid test piglets had lower
amounts of mitochondrial proteins than controls (P < 0.05) in all thre
e tissues, possibly reflecting reduced mitochondrial protein synthesis
during fetal life and suggesting that high postnatal T-3 levels did n
ot bring about major increases in protein synthesis within 24 h. Howev
er, test piglets exhibited higher rates of mitochondrial respiration t
han controls in liver and RH muscle, as shown by increases in State II
I and FCCP-stimulated respirations (P < 0.05), and mitochondrial CO an
d creatine kinase activities (P < 0.05). In RH muscle, both subsarcole
mmal and intermyofibrillar mitochondria showed the same trends. No cha
nges were observed in LD muscle. Our results describe for the first ti
me the effect of thyroid hormones on perinatal oxidative capacities an
d neonatal mitochondrial respiration in liver and skeletal muscle of t
he pig, through both the short-term regulation of mitochondrial respir
ation and the long-term control of mitochondrial biogenesis. The diffe
rential sensitivity of LD and RH muscles to thyroid hormones is discus
sed.